The invention relates to “active implantable medical devices” as defined by Directive 90/385/EEC of 20 Jun. 1990 the Council of the European Communities. The invention may relate to devices for cardiac pacing, resynchronization and/or defibrillation for diagnostics and treatment of cardiac arrhythmias, including active implants for purely diagnostic purposes. It relates in particular to preventive diagnosis of the risk of cardiac decompensation by methods of analysis algorithms of the signals collected by an implantable device. The diagnosis can be particularly useful with the implants implementing resynchronization functions.
Resynchronization is a technique called “CRT” (Cardiac Resynchronization Therapy) or “BVP” (Bi-Ventricular Pacing). This technique typically includes delivering a joint and continuous stimulation to the left and right ventricles, with potential application of a delay between the respective moments of stimulation. The delay is called interventricular delay or VVD. This delay is adjusted to resynchronize the contraction of both ventricles, which improves the hemodynamic status of the patient by optimizing the contraction/relaxation cycle with a direct benefit to the heart.
Long-term effects of the CRT therapy on heart failure patients, however, may be very different. These effects may be assessed by determining the left ejection fraction and the NYHA class of heart failure and the comparison of initial data with, for example, reassessed data after six months of treatment with CRT therapy.
An improved clinical status is found in the majority of patients (reflected by an increase in the left ejection fraction), while for some other patients, no significant improvement is seen. And yet, for some other patients there is, on the contrary, a worsening of the clinical condition, with decreased left ventricular ejection fraction, even with an increase in NYHA class.
Some of the patients that are non-responders to CRT therapy suffer from sleep apnea, more precisely central (non obstructive) apneas. Central apnea, which has a neurological cause and does not result from an obstacle to inspiration, may indeed appear as a result of heart failure. Therefore, the implementation of alerts concerning the risks of decompensation in heart failure patients with sleep apnea would allow changing and adapting without delaying treatment, and prevent hospitalizations.
EP 1433496 A1 (ELA Medical) discloses a device equipped with methods for measuring a parameter called HRV (Heart Rate Variability) to characterize the occurrence of episodes of apnea or hypopnea. The analysis is of the RR segment variability, thus purely in the temporal domain. This document also does not address in any way the question of heart failure patients.
EP 1413330 A1 (ELA Medical) proposes to monitor the signal of minute ventilation (MV signal) to detect the episodes of apnea or hypopnea and simultaneously assess the myocardial contractility, e.g. by analysis a transthoracic impedance signal or an endocardial acceleration signal. In case of significant variation in contractility during an apnea or hypopnea episode, the device temporarily modifies a pacing parameter, e.g. the frequency of stimulation or the atrioventricular delay in the case of a dual chamber device. This action can compensate the oxygen desaturation resulting from the failure of the sympathetic system activity during episodes of respiratory disorder, by increasing the flow. The purpose of this known device is to trigger a particular reaction of the device during the episodes of apnea only if this reaction is appropriate. The method does not include not a long-term monitoring of the clinical status of a heart failure patient, or the triggering of alerts in case of worsening of this clinical status proved in the long term.
EP 1741386 A1 (ELA Medical) describes a device wherein the occurrence of episodes of apnea is not detected by analysis of a MV or transthoracic impedance signal, but by that of an endocardial acceleration (EA) signal. A sudden depression of cardiac contractility, associated with the occurrence of an apnea or hypopnea, activates an alert that can be used to initiate appropriate therapy (increase in pacing rate) and/or document diagnosis episode information in a memory of the device: marker of occurrence of apnea, duration of the alert, or other information.
EP 1741387 A1 (ELA Medical) describes a device of the same type, operating from an external device including a cardiophonographic sensor pressed against the chest wall and an EEG machine, therefore applicable to patients not implanted with a cardiac pacemaker. In any event, this document does not address the specific problem of the diagnosis of heart failure.
EP 1867360 A2 (ELA Medical) proposes to combine between them various signals from an activity sensor (G sensor, accelerometer), a physiological sensor (MV sensor, minute ventilation) and an endocardial acceleration sensor (EA sensor). Algorithms of the respective analysis each produce a warning signal of cardiac decompensation and cross-analysis methods provide a composite signal of preventive alert, on different levels, depending on a number of specific indexes that may reveal a worsening of the clinical condition of the patient.
However, this approach does not aim to evaluate the effectiveness of CRT therapy, and shows no particular sensitivity or specificity for patients who are non-responders to CRT therapy, which is the main problem to be solved by embodiments of the present invention. Indeed, besides the fact that this known technique does not attempt to detect the possible occurrence of episodes of sleep apnea, the overall evaluated clinical condition is sensitive to factors such as the general activity level of the patient, the goal being to detect and take into account any reductions in activity when the patient spares himself after he has experienced first crisis occurring during exercise. But these factors are not significant when the deterioration in cardiac status is correlated with disturbances of sleep apnea; they may even prevent early detection of risk of cardiac decompensation, in particular in cases wherein the patient maintains a stable level of activity as long as he is not faced with a sudden worsening of his condition.